A number of physiological and psychological changes occur as we age, and many studies have shown that our gut microbiome also changes as we grow older. A fascinating new study is suggesting that a shift in gut bacteria in our middle-age could trigger a process that plays a role in cognitive decline in our later years. And diet may be the key to encouraging the growth of beneficial bacteria that benefit healthy brain aging.
UCLA researchers have discovered a new way to activate the stem cells in the hair follicle to make hair grow. The research, led by scientists Heather Christofk and William Lowry, may lead to new drugs that could promote hair growth for people with baldness or alopecia, which is hair loss associated with such factors as hormonal imbalance, stress, aging or chemotherapy treatment.
The research was published in the journal Nature Cell Biology.
Hair follicle stem cells are long-lived cells in the hair follicle; they are present in the skin and produce hair throughout a person’s lifetime. They are “quiescent,” meaning they are normally inactive, but they quickly activate during a new hair cycle, which is when new hair growth occurs. The quiescence of hair follicle stem cells is regulated by many factors. In certain cases they fail to activate, which is what causes hair loss.
Choriocapillary loss is a major cause of neovascular age-related macular degeneration (NV-AMD). Although vascular endothelial growth factor (VEGF) blockade for NV-AMD has shown beneficial outcomes, unmet medical needs for patients refractory or tachyphylactic to anti-VEGF therapy exist. In addition, the treatment could exacerbate choriocapillary rarefaction, necessitating advanced treatment for fundamental recovery from NV-AMD. In this study, Tie2 activation by angiopoietin-2–binding and Tie2-activating antibody (ABTAA) presents a therapeutic strategy for NV-AMD. Conditional Tie2 deletion impeded choriocapillary maintenance, rendering eyes susceptible to NV-AMD development. Moreover, in a NV-AMD mouse model, ABTAA not only suppressed choroidal neovascularization (CNV) and vascular leakage but also regenerated the choriocapillaris and relieved hypoxia. Conversely, VEGF blockade degenerated the choriocapillaris and exacerbated hypoxia, although it suppressed CNV and vascular leakage. Together, we establish that angiopoietin-Tie2 signaling is critical for choriocapillary maintenance and that ABTAA represents an alternative, combinative therapeutic strategy for NV-AMD by alleviating anti-VEGF adverse effects.
Neovascular age-related macular degeneration (NV-AMD) is a leading cause of irreversible vision loss among elderly persons in developed countries. NV-AMD is characterized by the formation of choroidal neovascularization (CNV), an ingrowth of abnormal blood vessels from the choroid through Bruch’s membrane into the sub-retinal pigment epithelium (RPE) or subretinal space. Throughout this ingrowth, abnormal leakages of fluids and bloods occur into the retina, causing vision distortion and loss of central vision (2, 3). To treat neovascular eye diseases including NV-AMD, anti–vascular endothelial growth factor A (VEGF) therapy has largely been used based on the fact that an excessive production of VEGF from hypoxic cells in the retino-choroidal complex is critical in the pathogenesis and features of neovascular eye diseases (3, 4).
Posted in cryonics, life extension
In a recent study, researchers have explored senescence-related proteins and protein interactions in cataracts, a leading cause of visual impairment and blindness in older adults.
Cataracts are characterized by the clouding of the lens in the eye, which leads to impaired vision. Cataracts generally develop slowly and can affect either one or both eyes at the same time. Cataract symptoms typically include faded colors, blurry or double vision, halos around light, trouble with bright lights, and difficulty seeing at night.
By analyzing proteins and their interactions, these researchers aim for a full understanding of this condition, showing that multiple biomarkers associated with aging rise during the formation of cataracts. Typically, p53, a well-known biomarker for the presence of senescent cells, is seen to rise along with transforming growth factor-beta1 (TGF-β1), another biomarker commonly associated with inflammation when encountered in high amounts. During the development of cataracts, the number of senescent cells rises, as this research shows.
Researchers at the Icahn School of Medicine at Mount Sinai have demonstrated that stem cells derived from the placenta known as Cdx2 cells can regenerate healthy heart cells after heart attacks in animal models. The findings, published in the May 20 issue of Proceedings of the National Academy of Sciences (PNAS), may represent a novel treatment for regenerating the heart and other organs.
“Cdx2 cells have historically been thought to only generate the placenta in early embryonic development, but never before were shown to have the ability to regenerate other organs, which is why this is so exciting. These findings may also pave the way to regenerative therapy of other organs besides the heart,” said principal investigator Hina Chaudhry, MD, Director of Cardiovascular Regenerative Medicine at the Icahn School of Medicine at Mount Sinai. “They almost seem like a super-charged population of stem cells, in that they can target the site of an injury and travel directly to the injury through the circulatory system and are able to avoid rejection by the host immune system.”
This team of Mount Sinai researchers had previously discovered that a mixed population of mouse placental stem cells can help the hearts of pregnant female mice recover after an injury that could otherwise lead to heart failure. In that study, they showed that the placental stem cells migrated to the mother’s heart and directly to the site of the heart injury. The stem cells then programmed themselves as beating heart cells to help the repair process.
Conclusion
As Nvidia CEO Jensen Huang has stated, “Software ate the world, but AI is going to eat software.” Extrapolating this statement to a more immediate implication, AI will first eat healthcare, resulting in dramatic acceleration of longevity research and an amplification of the human healthspan.
Next week, I’ll continue to explore this concept of AI systems in healthcare.
